Polyclonal antibodies against the NB1-bearing 58- to 64-kDa glycoprotein of human neutrophils do not identify an NB2-bearing molecule

The neutrophil-specific NB antigen system has been serologically characterized with human alloantisera. Two alleles, NB1 and NB2, have been described; however, there may be important quantitative or qualitative variation in the expression of NB1 and NB2. Human alloantibodies have been used to identify the 58- to 64-kDa glycoprotein (GP) on which NB1 antigen is located, but an NB2 antigen- bearing molecule has not yet been identified. To identify the NB2 molecule, human alloantibody to NB1 was used to isolate the 58- to 64- kDa NB1 GP, and rabbits were immunized with this GP. Two rabbit antisera were produced. Both antisera immunoblotted and immunoprecipitated the 58- to 64-kDa GP on which NB1 is located, but neither identified the molecule on which NB2 is located. The inability of two rabbit polyclonal antibodies specific for the NB1 molecule to react with the NB2-bearing molecule suggests that considerable differences may exist between these two molecules or that NB2 as currently defined is not related to NB1.     

Mathematical and computer modeling of acute normovolemic hemodilution

BACKGROUND: Advocates of acute normovolemic hemodilution (ANH) frequently neglect to consider the decreasing hematocrit of the patient during both hemodilution and the subsequent operative procedure and the need to begin transfusion at some minimal hematocrit. STUDY DESIGN AND METHODS: For more accurate prediction of the efficacy of ANH, equations were derived and a computer model developed that allowed accounting for the decreasing hematocrit due to blood loss in an isovolemic patient and calculating the red cell volume on a minute-by-minute basis; the model also began the transfusion of ANH blood on a mL-for-mL basis when the minimal hematocrit was reached and transfused any remaining blood following completion of the case. The red cell volume saved by performing ANH for a given estimated blood volume (EBV) was expressed as either the fraction of the red cell volume of a routinely banked unit of blood (red cells stored in additive solution: volume 350 mL, hematocrit 0.65) or the number of units saved. RESULTS: The number of units saved in a typical example–EBV, 5000 mL; pre-ANH hematocrit, 0.40; minimal hematocrit at which transfusion was begun, 0.25 over a range of estimated blood losses (500-2500 mL); and 1 to 5 ANH units drawn–never exceeded 0.6. Even with extensive hemodilution, as in a child (EBV, 1500 mL; pre-ANH hematocrit, 0.40; minimal hematocrit at which transfusion was begun, 0.15; 5 units drawn; and estimated blood losses, 2500, 1500, and 1000 mL) with a postdilution hematocrit of 0.16, the savings would have been only 0.29, 0.44, and 0.49 units, respectively. CONCLUSION: Because of the decreasing hematocrit in a bleeding isovolemic patient and the need to begin transfusion at some minimal hematocrit, the theoretic savings in red cell volume attributable to ANH is less than had previously been appreciated, and additional ANH does not necessarily result in additional patient benefit.     

Invalidation of antiglobulin tests by a high thermal amplitude cryoglobulin

A multiply transfused patient was referred for evaluation of a transfusion reaction. The direct and indirect antiglobulin tests (DAT, IAT) for alloantibody were negative. However, IgG-coated control cells failed to agglutinate in the negative reactions, casting doubt on their validity. At 4 degrees C, the patient's serum exhibited a large cryoprecipitate (2.9 mg/mL), made up predominantly of an IgG kappa paraprotein and having trace amounts of IgM and C3. Clear serum separated at 37 degrees C became cloudy within 10 minutes at room temperature (RT); within 4 hours, approximately 60 percent of the total precipitable cryoprotein had precipitated. Red cells (RBCs) incubated in fresh serum that had cooled to RT or RBCs obtained from RT or refrigerated samples contained cryoprecipitate that sedimented with the RBCs during washing with RT saline. On resuspension, enough IgG cryoglobulin redissolved to neutralize completely the commercial anti-IgG reagents. If the patient's samples were maintained at 37 degrees C, cryoprecipitate did not form, and RBCs washed four times at 37 degrees C gave valid DAT and IAT reactions. The removal of all cryoprecipitate from the patient's serum by centrifugation after overnight incubation at 4 degrees C also made possible valid antibody screening and compatibility tests.     

The pivotal role of Bifida Ferment Lysate on reinforcing the skin barrier function and maintaining homeostasis of skin defenses in vitro

Background

The semiactive or inactive probiotics or their extracts used in dermatology have interesting properties to ameliorate signs of irritated skin and enhance the skin barrier. Bifidobacterium, as the most common probiotics, which has been found to be effective in reducing acne and improving the skin barrier function of atopic dermatitis. Bifida Ferment Lysate (BFL) can be obtained from Bifidobacterium by fermentation and extraction.

Purpose

In this study, we investigated the effect of a topically used BFL on the skin using in vitro evaluation methods.

Results

The results showed that upregulation of skin physical barrier gene (FLG, LOR, IVL, TGM1, and AQP3) and antimicrobial peptide gene (CAMP and hBD-2) in HaCaT cells by BFL might be responsible for skin barrier resistance. In addition, BFL had strong antioxidant properties representing a dose-dependent increasing of the scavenging capacity of DPPH, ABTS, hydroxyl, and superoxide radicals. BFL treatment also fundamentally inhibited the intracellular ROS and MDA production and improved the activities of antioxidant enzymes (CAT and GSH-Px) in H₂O₂-stimulated HaCaT cells. As a good immunomodulatory factor, BFL efficiently decreased the secretion of IL-8 and TNF-α cytokines, and COX-2 mRNA expression in LPS-induced THP-1 macrophages.

Conclusion

BFL can strengthen the skin barrier function and stimulate skin barrier resistance, to reinforce the skin against oxidative stress and inflammatory stimuli.     

Nocturnal blood pressure surge in seconds is associated with arterial stiffness independently of conventional nocturnal blood pressure variability in suspected obstructive sleep apnea patients

Nocturnal blood pressure (BP) surge in seconds (sec-surge), which is characterized as acute transient BP elevation over several tens of seconds is induced by obstructive sleep apnea (OSA) and OSA-related sympathetic hyperactivity. The authors assessed the relationship between sec-surge and arterial stiffness in 34 nocturnal hypertensive patients with suspected OSA (mean age 63.9 ± 12.6 years, 32.4% female). During the night, they had beat-by-beat (BbB) BP and cuff-oscillometric BP measurements, and brachial-ankle pulse wave velocity (baPWV) was assessed as an arterial stiffness index. Multiple linear regression analysis revealed that the upward duration (UD) of sec-surge was significantly associated with baPWV independently of nocturnal oscillometric systolic BP variability (β = .365, p = .046). This study suggests that the UD of sec-surge, which can only be measured using a BbB BP monitoring device, may be worth monitoring in addition to nocturnal BP level.     

Gait Asymmetry Variation in Kinematics,Kinetics, and Muscle Force along with the Severity Levels of Knee Osteoarthritis

Objective

Knee osteoarthritis (OA) patients exhibit greater gait asymmetry than healthy controls. However, gait asymmetry in kinematics, kinetics and muscle forces across patients with different severity levels of knee OA is still unknown. The study aimed to investigate the changes of gait asymmetry in lower limb kinematics, kinetics, and muscle force across patients with different severity levels of knee OA.

Methods

This is a cross-sectional study. From January 2020 to January 2021, 118 patients with symptomatic and radiographic medial knee OA were categorized into three groups using the Kellgren and Lawrence scale (mild: grade 1 and 2, n = 37; moderate: grade 3, n = 31; severe: grade 4, n = 50). During self-paced walking, marker trajectories and ground reaction forces data were recorded. Musculoskeletal simulations were used to determine gait kinematics, kinetics, and muscle force. One-way analysis of variance with Tukey's post-hoc test was used to evaluate group difference. Paired-sample t-test was used to compared the between-limb difference.

Results

In the Severe group, significantly greater asymmetry index in knee flexion/extension range of motion (45%) was observed with a greater value on the contralateral side (p < 0.01), compared to the Mild (15%) and Moderate (15%) groups. Significantly higher peak hip contact force (JCF) on the contralateral side was found in the Mild (more affected side: 3.80 ± 0.67 BW, contralateral side: 4.01 ± 0.58 BW), Moderate (more affected side: 3.67 ± 0.56 BW, contralateral side: 4.07 ± 0.81 BW), and Severe groups (more affected side: 3.66 ± 0.79 BW, contralateral side: 3.94 ± 0.64 BW) (p < 0.05). Significantly greater gluteus medius muscle force on the contralateral side was found in Mild (more affected side: 0.48 ± 0.09 BW, contralateral side: 0.52 ± 0.12 BW), Moderate (more affected side: 0.45 ± 0.10 BW, contralateral side: 0.51 ± 0.15 BW), and Severe groups (more affected side: 0.42 ± 0.15 BW, contralateral side: 0.47 ± 0.12 BW) (p < 0.05). The contralateral side showing significantly higher peak knee adduction moment and medial knee JCF was only observed in the Mild group (p < 0.05).

Conclusions

Gait asymmetry in kinematics and muscle forces increased from mild to severe knee OA. Asymmetrical gait pattern tends to transfer loads from the more affected side to the contralateral side. Peak hip JCF and gluteus medius muscle force can be used to detect this asymmetrical gait pattern in patients with knee OA, regardless of severity levels.